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Martina K. Brückner

Researcher at Leipzig University

Publications -  56
Citations -  3924

Martina K. Brückner is an academic researcher from Leipzig University. The author has contributed to research in topics: Neurodegeneration & Amyloid precursor protein. The author has an hindex of 32, co-authored 56 publications receiving 3652 citations.

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A humanized version of Foxp2 affects cortico-basal ganglia circuits in mice

TL;DR: In the striatum, a part of the basal ganglia affected in humans with a speech deficit due to a nonfunctional FOXP2 allele, it is found that medium spiny neurons have increased dendrite lengths and increased synaptic plasticity, suggesting that alterations in cortico-basal ganglia circuits might have been important for the evolution of speech and language in humans.
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Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele

TL;DR: Results provide direct evidence that neuronal reorganization is affected severely in patients with Alzheimer’s disease carrying the apoE ε4 allele, which might lead to a more rapid functional decompensation, thereby contributing to an earlier onset and more rapid progression of the disease.
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Changes in acetylcholinesterase and butyrylcholinesterase in Alzheimer's disease resemble embryonic development--a study of molecular forms.

TL;DR: The degeneration of the cholinergic cortical afferentation in AD as reflected by a decrease of AChE G4 is accompanied by the process of a neuritic sprouting response involved in plaque formation which is probably associated with the expression of a developmental form of the enzyme.
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Perineuronal nets potentially protect against oxidative stress

TL;DR: It is shown that neurons ensheathed by a perineuronal net in the human cerebral cortex are less frequently affected by lipofuscin accumulation than neurons without a net both in normal-aged brain and Alzheimer's disease (AD).
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Activities of key glycolytic enzymes in the brains of patients with Alzheimer's disease.

TL;DR: It is suggested that the increased activity of some glycolytic enzymes may be, at least in part, the result of the reactive astrocytosis developing in the course of AD.